Assessment of a genetic contribution to osteoarthritis of the hip: sibling study
BMJ 2000; 321 doi: https://doi.org/10.1136/bmj.321.7270.1179 (Published 11 November 2000) Cite this as: BMJ 2000;321:1179All rapid responses
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Editor - I read the article by Lanyon and colleagues initially with
great enthusiasm, relating to the implication of genetic factors in hip
osteoarthritis1.
However, I am uncertain just how ethical it is to subject more than
600 healthy participants (siblings of their original cohort) to pelvic
radiographs. The authors' only purpose of using radiographs was as a
diagnostic tool. Rather than this, clinical examination using the Harris
Hip Score would have more accurately obtained the diagnosis with the
addition of information concerning loss of function and disease severity.
Examination of the patient would have detected and excluded those patients
with rheumatoid arthritis.
Despite the use of radiographs in this study, a great opportunity was
missed: no information concerning the morphology of the hip joints was
given. It would have been fascinating to measure the degree of femoral
head cover (CE angle), angle of acetabular inclination and femoral shaft
offset, which govern the magnitude and direction of forces and degree of
pressure concentration in the joint. Such morphological differences exist
between races and are believed to account for differences in prevalence of
OA and hip dysplasia2.
If Lanyon and colleagues had undertaken a morphological analysis,
finding no significant variations between the study and control groups
(presuming a similar racial breakdown in both groups, although this
information is not given), then rather than biomechanical and
morphological factors being responsible, articular collagen composition
(ie. biochemical factors) may be implicated. Obviously if collagen
composition predominates in influencing susceptibility then this may focus
treatment approaches in the future.
Unfortunately the study only succeeds in measuring the point
prevalence of OA in two selected groups, a figure more easily obtained by
simply comparing the rate of total hip replacement between them.
Did the ethics committee consult advice from specialists in
musculoskeletal medicine before approval?
References
1. Lanyon P et al. Assessment of a genetic contribution to
osteoarthritis of the hip: sibling study. BMJ 2000; 321:1179-83.
2. Fuji G, Funayama K, Benson M. Radiological measurement of the hip
joint: comparison between Japanese and British. British and Japanese
Orthopaedic Associations Combined Congress, London, 3-6 Oct 2000.
Iain Chambers Hip Research Fellow
Department of Orthopaedics,
Queen Elizabeth Hospital,
Gateshead NE9 6SX.
No competing interests.
Correspondence to:
Iain Chambers FRCS,
18 Cloverdale Gardens,
High Heaton,
Newcastle upon Tyne NE7 7QJ.
Competing interests: No competing interests
Assessment of a genetic contribution to osteoarthritis of the hip
The paper by Lanyon and colleagues1 adds further weight to the
genetic contribution to "primary" osteoarthritis of the hip. In a 1983
study2 of 341 such patients of both sexes aged 39-86 undergoing total hip
replacement in Oxford, matched with a control population of 7072 blood
donors from the same geographical catchment area, the relative frequencies
of blood groups O and A were found to be reversed in the two groups, Group
A being commoner than Group O in the osteoarthritis patients. When Group
O phenotype frequencies were compared with "non-O" (i.e. A, B and AB),
patients and controls differed significantly (chi-squared = 3.87).
All patients had radiological evidence of degenerative arthritis,
with confirmatory histological evidence from examination of the excised
femoral heads. All individuals within this clearly defined group were
included, as blood was routinely taken for cross-matching pre-operatively
in all cases. Lanyon and colleagues included both primary and revision
hip replacement patients in their study population, whose composition also
depended on response to a questionnaire. While their index participants
were a comparable group to those in the above blood group study, their
sibling and urography groups were only defined by radiographic and not
clinical evidence of arthritis.
Numerous insults to the hip such as trauma, infection, avascularity,
rheumatoid disease, or congenital abnormality are known precursors of
"secondary" arthritis. Such histories were excluded in the blood group
study population. The pathogenesis of "primary" osteoarthritis of the hip
remains elusive. Biochemical variations in cartilage metabolism under
genetic control may be responsible for susceptibility to arthritic change
in certain individuals, and the factors underlying the ABO polymorphism
play a fundamental role in the organisation of cell membranes. Further
large-scale studies will provide more information about the genetic
contribution to this common condition, but populations must be carefully
specified to include only those in whom there is no known predisposing
factor for arthritis, and who have clinical (and ideally histolgical) as
well as radiographic evidence of the disease.
1 Lanyon P, Muir K, Doherty S, Doherty M. Assessment of a genetic
contribution to osteoarthritis of the hip: sibling study. BMJ 2000;
321:479-83 (11 November).
2 Lourie JA. Is there an association between ABO blood groups and
primary osteoarthrosis of the hip? Ann Hum Biol 1983; 10:381-4.
Competing interests: No competing interests